<?xml version="1.0" encoding="UTF-8" standalone="no" ?>
<rss version="2.0">
  <channel>
    <title>Ruitenberg, A.</title>
    <link>http://repub.eur.nl/res/aut/3801/</link>
    <description>List of Publications</description>
    <language>en</language>
    <image>
      <url>http://repub.eur.nl/static-eur/img/logo.png</url>
      <title>RePub, Erasmus University Rotterdam</title>
      <link>http://repub.eur.nl</link>
    </image>
    <item>
      <title>Bilateral caudate nucleus infarction associated with variant in circle of Willis (Article)</title>
      <link>http://repub.eur.nl/res/pub/35141/</link>
      <pubDate>2007-11-01T00:00:00Z</pubDate>
      <description></description>
    </item> <item>
      <title>The electrophysiological muscle scan (Article)</title>
      <link>http://repub.eur.nl/res/pub/35724/</link>
      <pubDate>2007-10-01T00:00:00Z</pubDate>
      <description>This study aims to assess the potential of the electrophysiological muscle scan or stimulus-response curve as a diagnostic instrument. If stimulus intensity is gradually increased from subthreshold to supramaximal values, all motor units in a muscle are successively activated. Thus, by plotting response size versus stimulus intensity, an impression (scan) of the entire muscle can be obtained. We recorded 54 detailed scans from 34 patients and 11 healthy subjects, and analyzed them visually and quantitatively. The scan summarized much diagnostic information in a single picture. Specific patterns in or properties of the scan (steps, maximum, variability, decrements, stimulus intensities used) provide clinically relevant information regarding motor unit number, size, and stability, and neuromuscular transmission and axonal excitability. The scan can be recorded noninvasively in about 5 minutes and is fairly easy to interpret. Because it is built up from contributions of all functioning motor units, the scan shows if and how many large motor units are present. There is no sample bias. For these reasons, further exploration and exploitation of this tool in the clinical setting are warranted. </description>
    </item> <item>
      <title>Inflammatory proteins in plasma and the risk of dementia: the rotterdam study. (Article)</title>
      <link>http://repub.eur.nl/res/pub/13377/</link>
      <pubDate>2004-05-01T00:00:00Z</pubDate>
      <description>BACKGROUND: Increased levels of inflammatory proteins have been found in
      the brains and plasma samples of patients with dementia. Whether the
      levels of inflammatory proteins in plasma samples are elevated before
      clinical onset of dementia is unclear. OBJECTIVE: To determine whether
      high levels of inflammatory proteins in plasma samples are associated with
      an increased risk of dementia. DESIGN AND SETTING: A case-cohort study
      within the Rotterdam Study, a population-based prospective cohort study in
      the Netherlands. PARTICIPANTS: The source population comprises 6713
      subjects who, at baseline (1990-1993), were free of dementia and underwent
      venipuncture. From these, we selected both a random subcohort of 727
      subjects and 188 cases who had developed dementia at follow-up. MAIN
      OUTCOME MEASURES: The associations between plasma levels of
      alpha1-antichymotrypsin, C-reactive protein, interleukin 6, the soluble
      forms of intercellular adhesion molecule-1, and vascular cell adhesion
      molecule-1 and the risk of dementia were examined using the Cox
      proportional hazards regression models. RESULTS: High levels of
      alpha1-antichymotrypsin, interleukin 6, and, to a lesser extent,
      C-reactive protein were associated with an increased risk of dementia;
      rate ratios per standard deviation increase were 1.49 (95% confidence
      interval, 1.23-1.81), 1.28 (95% confidence interval, 1.06-1.55), and 1.12
      (95% confidence interval, 0.99-1.25), respectively. Similar associations
      were observed for Alzheimer disease, whereas rate ratios of vascular
      dementia were higher for alpha1-antichymotrypsin and C-reactive protein.
      Soluble forms of intercellular adhesion molecule-1 and vascular cell
      adhesion molecule-1 were not associated with dementia. CONCLUSION: Plasma
      levels of inflammatory proteins are increased before clinical onset of
      dementia, Alzheimer disease, and vascular dementia.</description>
    </item> <item>
      <title>Alcohol consumption and risk of dementia: the Rotterdam Study (Article)</title>
      <link>http://repub.eur.nl/res/pub/5864/</link>
      <pubDate>2002-01-26T00:00:00Z</pubDate>
      <description>BACKGROUND: Light-to-moderate alcohol consumption reduces the risk of coronary heart disease and stroke. Because vascular disease is associated with cognitive impairment and dementia, we hypothesised that alcohol consumption might also affect the risk of dementia. METHODS: We examined the relation between alcohol consumption and risk of dementia in individuals taking part in the Rotterdam Study--a prospective population-based study of 7983 individuals aged 55 years and older. We studied all participants who did not have dementia at baseline (1990-93) and who had complete data on alcohol consumption (n=5395). Through follow-up examinations in 1993-94 and 1997-99 and an extensive monitoring system, we obtained nearly complete follow-up (99.7%) until the end of 1999. We used proportional hazards regression analysis, adjusted for age, sex, systolic blood pressure, education, smoking, and body-mass index, to compare the risk of developing dementia between individuals who regularly consumed alcohol and individuals who did not consume alcohol. FINDINGS: The average follow-up was 6.0 years. During this period, 197 individuals developed dementia (146 Alzheimer's disease, 29 vascular dementia, 22 other dementia). The median alcohol consumption was 0.29 drinks per day. Light-to-moderate drinking (one to three drinks per day) was significantly associated with a lower risk of any dementia (hazard ratio 0.58 [95% CI 0.38-0.90]) and vascular dementia (hazard ratio 0.29 [0.09-0.93]). We found no evidence that the relation between alcohol and dementia varied by type of alcoholic beverage. INTERPRETATION: These findings suggest that light-to-moderate alcohol consumption is associated with a reduced risk of dementia in individuals aged 55 years or older. The effect seems to be unchanged by the source of alcohol.</description>
    </item> <item>
      <title>Dietary intake of antioxidants and risk of Alzheimer disease (Article)</title>
      <link>http://repub.eur.nl/res/pub/9925/</link>
      <pubDate>2002-01-01T00:00:00Z</pubDate>
      <description>CONTEXT: Laboratory findings have suggested that oxidative stress may
      contribute to the pathogenesis of Alzheimer disease. Therefore, the risk
      of Alzheimer disease might be reduced by intake of antioxidants that
      counteract the detrimental effects of oxidative stress. OBJECTIVE: To
      determine whether dietary intake of antioxidants is related to risk of
      Alzheimer disease. DESIGN AND SETTING: The Rotterdam Study, a
      population-based, prospective cohort study conducted in the Netherlands.
      PARTICIPANTS: A total of 5395 participants who, at baseline (1990-1993),
      were aged at least 55 years, free of dementia, and noninstitutionalized
      and had reliable dietary assessment. Participants were reexamined in
      1993-1994 and 1997-1999 and were continuously monitored for incident
      dementia. MAIN OUTCOME MEASURES: Incidence of Alzheimer disease, based on
      Diagnostic and Statistical Manual of Mental Disorders, Revised Third
      Edition (DSM-III-R) criteria and National Institute of Neurological and
      Communicative Disorders and Stroke and Alzheimer Disease and Related
      Disorders Association (NINCDS-ADRDA) criteria, associated with dietary
      intake of beta carotene, flavonoids, vitamin C, and vitamin E. RESULTS:
      After a mean follow-up of 6 years, 197 participants developed dementia, of
      whom 146 had Alzheimer disease. When adjustments were made for age, sex,
      baseline Mini-Mental State Examination score, alcohol intake, education,
      smoking habits, pack-years of smoking, body mass index, total energy
      intake, presence of carotid plaques, and use of antioxidative supplements,
      high intake of vitamin C and vitamin E was associated with lower risk of
      Alzheimer disease (rate ratios [RRs] per 1-SD increase in intake were 0.82
      [95% confidence interval [CI], 0.68-0.99] and 0.82 [95% CI, 0.66-1.00],
      respectively). Among current smokers, this relationship was most
      pronounced (RRs, 0.65 [95% CI, 0.37-1.14] and 0.58 [95% CI, 0.30-1.12],
      respectively) and also was present for intake of beta carotene (RR, 0.49
      [95% CI, 0.27-0.92]) and flavonoids (RR, 0.54 [95% CI, 0.31-0.96]). The
      associations did not vary by education or apolipoprotein E genotype.
      CONCLUSION: High dietary intake of vitamin C and vitamin E may lower the
      risk of Alzheimer disease.</description>
    </item> <item>
      <title>Nonsteroidal antiinflammatory drugs and the risk of Alzheimer's disease (Article)</title>
      <link>http://repub.eur.nl/res/pub/8454/</link>
      <pubDate>2001-01-01T00:00:00Z</pubDate>
      <description>BACKGROUND: Previous studies have suggested that the use of nonsteroidal antiinflammatory drugs (NSAIDs) may help to prevent Alzheimer's disease. The results, however, are inconsistent. METHODS: We studied the association between the use of NSAIDs and Alzheimer's disease and vascular dementia in a prospective, population-based cohort study of 6989 subjects 55 years of age or older who were free of dementia at base line, in 1991. To detect new cases of dementia, follow-up screening was performed in 1993 and 1994 and again in 1997 through 1999. The risk of Alzheimer's disease was estimated in relation to the use of NSAIDs as documented in pharmacy records. We defined four mutually exclusive categories of use: nonuse, short-term use (1 month or less of cumulative use), intermediate-term use (more than 1 but less than 24 months of cumulative use), and long-term use (24 months or more of cumulative use). Adjustments were made by Cox regression analysis for age, sex, education, smoking status, and the use or nonuse of salicylates, histamine Hz-receptor antagonists, antihypertensive agents, and hypoglycemic agents. RESULTS: During an average follow-up period of 6.8 years, dementia developed in 394 subjects, of whom 293 had Alzheimer's disease, 56 vascular dementia, and 45 other types of dementia. The relative risk of Alzheimer's disease was 0.95 (95 percent confidence interval, 0.70 to 1.29) in subjects with short-term use of NSAIDs, 0.83 (95 percent confidence interval, 0.62 to 1.11) in those with intermediate-term use, and 0.20 (95 percent confidence interval, 0.05 to 0.83) in those with long-term use. The risk did not vary according to age. The use of NSAIDs was not associated with a reduction in the risk of vascular dementia. CONCLUSIONS: The long-term use of NSAIDs may protect against Alzheimer's disease but not against vascular dementia.</description>
    </item> <item>
      <title>Reproductive period and risk of dementia in postmenopausal women (Article)</title>
      <link>http://repub.eur.nl/res/pub/9615/</link>
      <pubDate>2001-01-01T00:00:00Z</pubDate>
      <description>CONTEXT: Exogenous estrogen use may lower risk of dementia in postmenopausal women. A relationship between long-term exposure to endogenous estrogens and incident dementia has been hypothesized but not studied. OBJECTIVE: To determine whether a longer reproductive period, as an indicator of longer exposure to endogenous estrogens, is associated with lower risk of dementia and Alzheimer disease (AD) in women who have natural menopause. DESIGN AND SETTING: The Rotterdam Study, a population-based prospective cohort study conducted in the Netherlands. PARTICIPANTS: A total of 3601 women aged 55 years or older who did not have dementia at baseline (1990-1993) and had information on age at menarche, age at menopause, and type of menopause. Participants were reexamined in 1993-1994 and 1997-1999 and were continuously monitored for development of dementia. MAIN OUTCOME MEASURES: Incidence of dementia, based on Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition criteria, and AD, based on National Institute of Neurological Disorders and Stroke/Alzheimer's Disease and Related Disorders Association criteria, compared by quartiles of reproductive period among women with natural menopause. RESULTS: During 21 046 person-years of follow-up (median follow-up, 6.3 years), 199 women developed dementia, including 159 who developed AD. After adjusting for age, dementia was not clearly associated with length of reproductive period. However, after adjusting for multiple covariates, women with natural menopause and more reproductive years had an increased risk of dementia (adjusted rate ratio [RR] for women with &gt;39 reproductive years [highest quartile] compared with &lt;34 reproductive years [lowest quartile], 1.78; 95% confidence interval [CI], 1.12-2.84). The adjusted RR per year of increase was 1.04 (95% CI, 1.01-1.08). For risk of AD, the adjusted RRs were 1.51 (95% CI, 0.91-2.50) and 1.03 (95% CI, 1.00-1.07), respectively. Risk of dementia associated with a longer reproductive period was most pronounced in APOE epsilon4 carriers (adjusted RR for &gt;39 reproductive years compared with &lt;34 reproductive years, 4.20 [95% CI, 1.97-8.92] for dementia and 3.42 [95% CI, 1.51-7.75] for AD), whereas in noncarriers, no clear association with dementia or AD was observed. CONCLUSION: Our findings do not support the hypothesis that a longer reproductive period reduces risk of dementia in women who have natural menopause.</description>
    </item> <item>
      <title>Vascular factors in dementia: observations in the Rotterdam Study (Doctoral Thesis)</title>
      <link>http://repub.eur.nl/res/pub/20397/</link>
      <pubDate>2000-12-13T00:00:00Z</pubDate>
      <description></description>
    </item>
  </channel>
</rss>